This article reviews the production of different phenotypes from the same genotype in the same environment by stochastic cellular events, nonlinear mechanisms during patterning and morphogenesis, and probabilistic self-reinforcing circuitries in the adult life. These aspects of phenotypic variation are summarized under the term ‘stochastic developmental variation’ (SDV) in the following. In the past, SDV has been viewed primarily as a nuisance, impairing laboratory experiments, pharmaceutical testing, and true-to-type breeding. This article also emphasizes the positive biological effects of SDV and discusses implications for genotype-to-phenotype mapping, biological individuation, ecology, evolution, and applied biology. There is strong evidence from experiments with genetically identical organisms performed in narrowly standardized laboratory set-ups that SDV is a source of phenotypic variation in its own right aside from genetic variation and environmental variation. It is obviously mediated by molecular and higher-order epigenetic mechanisms. Comparison of SDV in animals, plants, fungi, protists, bacteria, archaeans, and viruses suggests that it is a ubiquitous and phylogenetically old phenomenon. In animals, it is usually smallest for morphometric traits and highest for life history traits and behaviour. SDV is thought to contribute to phenotypic diversity in all populations but is particularly relevant for asexually reproducing and genetically impoverished populations, where it generates individuality despite genetic uniformity. In each generation, SDV produces a range of phenotypes around a well-adapted target phenotype, which is interpreted as a bet-hedging strategy to cope with the unpredictability of dynamic environments. At least some manifestations of SDV are heritable, adaptable, selectable, and evolvable, and therefore, SDV may be seen as a hitherto overlooked evolution factor. SDV is also relevant for husbandry, agriculture, and medicine because most pathogens are asexuals that exploit this third source of phenotypic variation to modify infectivity and resistance to antibiotics. Since SDV affects all types of organisms and almost all aspects of life, it urgently requires more intense research and a better integration into biological thinking.

Rapidly growing trade of ornamental animals may represent an entry pathway for emerging pathogens; this may concern freshwater crayfish that are increasingly popular pets. Infected crayfish and contaminated water from aquaria may be released to open waters, thus endangering native crustacean fauna. We tested whether various non-European crayfish species available in the pet trade in Germany and the Czech Republic are carriers of two significant crustacean pathogens, the crayfish plague agent Aphanomyces astaci and the white spot syndrome virus (WSSV). The former infects primarily freshwater crayfish (causing substantial losses in native European species), the latter is particularly known for economic losses in shrimp aquacultures. We screened 242 individuals of 19 North American and Australasian crayfish taxa (the identity of which was validated by DNA barcoding) for these pathogens, using molecular methods recommended by the World Organisation for Animal Health. A. astaci DNA was detected in eight American and one Australian crayfish species, comprising in total 27 % of screened batches. Furthermore, viability of A. astaci was confirmed by its isolation to axenic cultures from three host taxa, including the parthenogenetic invader Marmorkrebs (Procambarus fallax f. virginalis). In contrast, WSSV was only confirmed in three individuals of Australian Cherax quadricarinatus. Despite modest prevalence of detected infections, our results demonstrate the potential of disease entry and spread through this pathway, and should be considered if any trade regulations are imposed. Our study highlights the need for screening for pathogens in the ornamental trade as one of the steps to prevent the transmission of emerging diseases to wildlife.